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Persistent intercoronary and intracoronary communications were observed on cineangiograms in four patients having vasospastic angina without significant coronary narrowings. On provocation of coronary spasm using ergonovine maleate, these communications seemed to protect myocardium from ischemia, at least partially.
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In order to determine the natural evolution of different clinical types of "unstable angina", 167 patients were included in a prospective study. After angiography, 11 (6.5%) were excluded because they had no significant coronary lesions. The remaining 156 were sorted into different groups according to their clinical characteristics and were followed up for a period of 24 months at least. After that follow-up period, mortality and incidence of acute myocardial infarction (AMI) were as follows: angina of recent onset (Class III--IV NYHA): 8.5% (3/35) and 34.2% (12/35). Progressive angina: 7.4% (2/27) and 7.4% (2/27). Intermediate syndrome: 41.6% (10/24) and 37.5% (9/24). Prinzmetal's angina: 10% (1/10) and 10% (1/10). Post acute myocardial infarction angina: 35% (7/20) and 10% (2/20). Acute persistent ischemia: 2.5% (1/40) and 20% (8/40). Comparison of these figures pointed out significant differences (p less than 0.001 for mortality and p less than 0.03 for AMI incidence respectively). We conclude that it is clinically possible to identify different groups within the so-called unstable angina. Such a division not only allows for the creation of more homogeneous groups, but it contributes to a more rational therapeutic approach and also permits identification of high risk prodromes of greater complications, such as myocardial infarction or sudden death.
A patient with a 5-year history of nonexertional episodic chest discomfort terminating in nausea presented with recurrent periods of marked ST elevations. Each observed episode terminated in the triad of bradycardia, hypotension, and nausea. ST elevation normalized almost immediately when this triad supervened. It is hypothesized that this represented activation of the Bezold-Jarisch reflex. Resolution may have been due to reflexly mediated parasympathetic coronary vasodilation. An episode of ST elevation occurred 24 h after admission which did not result in activation of the Bezold-Jarisch reflex. Following this latter episode, Q waves and enzymatic evidence of myocardial infarction were documented.
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Heart rate response to submaximal graded treadmill exercise was measured in 45 patients with vasospastic angina, 31 with effort angina, and 40 normal controls. There was no difference of resting heart rate among the three groups. Vasospastic angina showed significantly poor responsiveness of heart rate to exercise at every stage: stage 1, 2.5 km/h (10%), stage 3, 4.5 km/h (10%), stage 5, 5.5 km/h (14%), stage 7, 5.5 km/h (22%), when compared with those in normal controls. The effort angina group also showed lower heart rates at stages 3 and 5 than those in control subjects, although their heart rate at stage 1 was not different from that in normals. When abnormal response suggesting vasospastic angina was defined as heart rate at each stage lower than values of mean heart rate +/- 1 SD in normal controls, positive test results were obtained in 15 of 45 patients (33%). The use of heart rate criteria in addition to ischemic criteria raises sensitivity from 27 to 51% (p less than 0.02).
Exercise-induced ST-segment elevation usually occurs in patients with coronary artery disease. We report a case in which ST-segment elevation occurred during the recovery phase of exercise in a patient with normal coronary arteries.
We report the observation of a 62-year-old patient who was admitted for unstable angina. A prolonged chest pain (more than two hours) with a major electrocardiographic lesion in the posterior leads needed an urgent coronary arteriography in order to attempt a recanalization. Antecedents of arteriopathy of the lower limbs with aortobifemoral bypass required an axillary artery right side approach. A selective right coronary opacification showed complete occlusion at the junction of segments 1 and 2. An intracoronary injection of isosorbide dinitrate relieved a coronary spasm and allowed a complete visualization of the right coronary artery. This appeared to be very atherosclerotic with several severe narrowings, and a subocclusive lesion at the site of the initial occlusion. Percutaneous transluminal coronary angioplasties (PTCA) were performed and led to real 'restructuring' of the right coronary artery. The clinical outcome was excellent without recurrent angina pectoris. An angiographic control performed 6 months after PTCA demonstrated the persistence of the coronary recanalization and an evident improvement of the segmental contractility. This report emphasizes the role of coronary spasm in the genesis of myocardial infarction and shows that PTCA may be performed as a first approach at the acute phase of myocardial infarction; to our knowledge it is the first PTCA performed by an axillary approach at the acute stage of myocardial infarction.
The peak incidence of ventricular fibrillation in acute myocardial infarction usually occurs during the first hours after the onset. Electrophysiological changes immediately after the onset have been studied in animal models, but are still incompletely understood in humans. For clarification of the characteristic features of ventricular arrhythmias during acute myocardial ischemia, ventricular arrhythmias were studied in 81 patients with vasospastic angina pectoris induced by ergonovine. Ventricular arrhythmias occurred in 45 of these patients, including ventricular tachycardia in 15, and ventricular fibrillation requiring repeated DC defibrillation in two patients. Most ventricular extrasystoles occurred before the ST segment reached maximum elevation, while reperfusion arrhythmias were less common. In many patients the coupling intervals varied, and the configuration was multiform. It is concluded that ventricular arrhythmias occurring during ergonovine-induced coronary spasm show different characteristics from those occurring during chronic ischemia. As the arrhythmias in this study seem, in some ways, to resemble arrhythmias occurring at the onset of myocardial infarction, the results might provide useful information on ventricular arrhythmias in myocardial ischemia in humans.
Coronary bypass surgery is performed more frequently in men than in women. A selection bias in favor of men may exist in currently utilized evaluation precesses for patients with both chest pain syndromes and documented coronary artery disease. Surgery should be considered in women with significant left main coronary artery stenosis, "left main equivalent" coronary disease, severe three-vessel coronary disease with/without left ventricular dysfunction, two-vessel coronary disease (including a proximal left anterior descending artery stenosis), and unstable angina pectoris with decreased left ventricular function. Women and men undergoing coronary bypass surgery seem to benefit from internal mammary artery grafts used alone or in combination with saphenous vein grafts. Surgical mortality, incomplete revascularization, early and late graft occlusion, and recurrent angina are more prevalent in women who undergo surgery. However, long-term mortality following surgery is similar in men and women.
This report presents a case of paradoxical coronary arterial dilation induced by intracoronary ergonovine. When compared with the control angiogram, the right coronary artery obviously dilated with selective, intracoronary administration of cumulative doses of 5 micrograms and 15 micrograms ergonovine without concomitant hemodynamic changes. Additional intracoronary infusion of 35 micrograms ergonovine into the right coronary artery inversely increased vascular tone of the vessel associated with a focal hyperconstriction. Such a biphasic response of arterial diameter to intracoronary ergonovine was also observed in the left coronary artery, but the degree of dilation was much smaller.
Recently, the presence of vasospasm in small coronary arteries is speculated in animals and humans. A 40-year-old female patient complained of chest pain at rest. Left ventriculogram showed normal wall motions. Left and right coronary arteries were also normal. After methylergometrine maleate was selectively administered to a right coronary artery, she complained of chest pain, and ST-segment elevation was detected in leads II, III, and aVF of ECG. Right coronary arteriography was performed immediately, but no coronary stenosis was found. The next day, methylergometrine maleate was again administered intravenously and the patient complained of chest pain, but no ischemic changes were observed in ECG. Thallium-201 myocardial scintigraphy followed immediately. Apical perfusion defect was detected in stress image. In the delayed image, it showed complete redistribution. Three days later, catheterization and scintigraphy were performed at the same time. When methylergometrine maleate was administered to the left coronary artery, she complained of chest pain within a few minutes of the injection; however, ECG remained unchanged. 201Tl myocardial scintigraphy was performed immediately. In the stress image, it showed apical perfusion defect as shown in the intravenous methylergometrine maleate injection study. It also showed complete redistribution in the delayed image. Apical perfusion defect can be attributed to myocardial ischemia of left coronary artery, which are too small to be detected by conventional coronary arteriography. Vasospasm in small coronary arteries may be involved in this phenomenon.
Dobutamine stress echocardiography (DSE) has been widely used for the noninvasive diagnosis of obstructive coronary artery disease. The ST-segment elevation during DSE has been reported as an infrequent event, caused by old myocardial infarction and/or critical coronary narrowings. The patient presented here was a 35-year-old man with a recent history of nonexertional chest pain. He had hypercholesterolemia and a history of heavy smoking as risk factors. The patient developed ST-segment elevation with chest pain during 40 mcg/min dobutamine infusion for the stress echocardiographic examination. Subsequent coronary angiograms revealed only mild coronary atherosclerosis. It is speculated that coronary spasm occurred in this patient as a paradoxical response to increased coronary blood flow with dobutamine administration.
The development of an intravenous form of nitroglycerin has further enhanced the role of nitrates in the therapy of cardiovascular disorders. This new preparation permits prompt initiation of therapy and rapid attainment of high systemic levels; because of its short half-life, rapid dose titration is both feasible and safe. The antianginal effects of intravenous nitroglycerin are useful in the treatment of coronary vasospasm and unstable angina pectoris. Its hemodynamic effects are of benefit in the therapy of congestive heart failure and in the control of peri-operative hypertension. Recent data suggest that, with appropriate monitoring, intravenous nitroglycerin can be safely administered to patients with evolving myocardial infarction to reduce the extent of myocardial damage.
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The very first presentation of ischemic heart disease--acute infarction, sudden death, or unstable angina--most often occurs abruptly. The first approximation that it occurs as a random event only when a certain "threshold severity" of coronary atherosclerosis has gradually developed, although widely accepted, should perhaps be reconsidered and expanded on the basis of the following considerations. Acute coronary occlusion leading to myocardial infarction often occurs at the site of mild or noncritical coronary stenoses. Conversely, in patients with chronic angina severe coronary stenoses can remain unchanged for years with no detectable progression. When a coronary artery occludes, the size of infarction can vary greatly, and when ischemia and infarction occur, malignant arrhythmias occur in some patients but not in others. Thus, in a second approximation, ischemic heart disease should be considered as the result of the variable combination of three major components: a) A very variable chronic atherosclerotic background, which can result from a variety of pathologic processes; b) A number of acute ischemic stimuli, which can unpredictably impair myocardial blood flow as a result of coronary thrombosis and/or vasoconstriction; c) A variable response of the heart to a sudden reduction of coronary blood flow in terms of collateral perfusion and malignant arrhythmias. Therefore, at one extreme end of the spectrum in any individual, ischemic syndromes may present predominantly as a result of an extremely large chronic background component. At the other extreme, powerful acute ischemic stimuli can unexpectedly impair blood supply by coronary thrombosis, constriction, or their combination, in the presence of a mild chronic atherosclerotic background.(ABSTRACT TRUNCATED AT 250 WORDS)
A 34-year-old man presenting with angina both at rest and on exertion was investigated. He developed severe ST segment elevation and a brief period of ventricular tachycardia during an exercise tolerance test. On coronary angiography, 60% fixed luminal narrowing was observed in the proximal left anterior descending coronary artery and a severe spasm developed at this site, leading to temporary total occlusion of the vessel. Successful coronary angioplasty (PTCA) was performed on this lesion, with a residual 15% narrowing. However, the patient had a recurrence of angina 3 weeks later, despite being administered high doses of nitrate and calcium antagonist. During control angiography, the lesion severity was unchanged, but spasm developed again following contrast injection. At this time, a Palmaz-Schatz stent was implanted. Calcium antagonist, nitrate, Ticlopidine and low molecular weight heparin therapy was started. There was no recurrence of symptoms during a 3-month follow-up. The exercise tolerance test, and myocardial perfusion scintigraphy findings were normal and the stent was patent without restenosis at the end of the 3-month follow-up. Intracoronary stent implantation for persistent coronary spasm refractory to conventional medical therapy can be considered a feasible and attractive treatment modality for the control of symptoms.